Time‐varying correlations between delta EEG power and heart rate variability in midlife women: The SWAN Sleep Study

No studies have evaluated the dynamic, time‐varying relationship between delta electroencephalographic (EEG) sleep and high frequency heart rate variability (HF‐HRV) in women. Delta EEG and HF‐HRV were measured during sleep in 197 midlife women (M_age = 52.1, SD = 2.2). Delta EEG–HF‐HRV correlations in nonrapid eye movement (NREM) sleep were modeled as whole‐night averages and as continuous functions of time. The whole‐night delta EEG–HF‐HRV correlation was positive. The strongest correlations were observed during the first NREM sleep period preceding and following peak delta power. Time‐varying correlations between delta EEG–HF‐HRV were stronger in participants with sleep‐disordered breathing and self‐reported insomnia compared to healthy controls. The dynamic interplay between sleep and autonomic activity can be modeled across the night to examine within‐ and between‐participant differences including individuals with and without sleep disorders.     

Cognitive effects of genetic variation in monoamine neurotransmitter systems: A population‐based study of COMT,MAOA, and 5HTTLPR

Individual differences in cognitive function are highly heritable and most likely driven by multiple genes of small effect. Well‐characterized common functional polymorphisms in the genes MAOA, COMT, and 5HTTLPR each have predictable effects on the availability of the monoamine neurotransmitters dopamine, noradrenaline, and serotonin. We hypothesized that 5HTTLPR genotype would show little association with prefrontal cognitive performance, but that COMT and MAOA would have interacting effects on cognition through their shared influence on prefrontal catecholamine availability. We assessed the individual and epistatic effects of functional polymorphisms in COMT, MAOA, and 5HTTLPR on children's prefrontal cognitive function in nearly 6,000 children from the population‐based Avon Longitudinal Study of Parents and Children (ALSPAC). Neither MAOA nor 5HTTLPR polymorphisms showed significant effects on cognitive function. In boys but not girls, there was a modest but statistically significant interaction between MAOA and COMT genotypes such that increased prefrontal catecholamine availability was associated with better working memory. These results suggest that assessment of multiple genes within functionally related systems may improve our understanding of the genetic basis of cognition. © 2010 Wiley‐Liss, Inc.     

Evidence that brain glucose availability influences exercise‐enhanced extracellular 5‐HT level in hippocampus: a microdialysis study in exercising rats

The relationship between brain glucose and serotonin is still unclear and no direct evidence of an action of brain glucose on serotonergic metabolism in central fatigue phenomena has been shown yet. In order to determine whether or not brain glucose could influence the brain 5‐hydroxytryptamine (5‐HT) system, we have monitored in microdialysis the effects of a direct injection of glucose in rat brain hippocampus on serotonergic metabolism [i.e. 5‐HT, 5‐hydroxyindoleacetic acid (5‐HIAA) and tryptophan (TRP)], during high intensive treadmill running. The injection was performed just before and after exercise. We have shown that glucose induced a decrease of brain 5‐HT levels to a minimum of 73.0 ± 3.5% of baseline after the first injection (P < 0.01) and to 68.5 ± 5.5% of baseline after the second injection (P < 0.01) and consequently prevented the exercise‐induced 5‐HT enhanced levels. We have observed the same phenomenon concerning the 5‐HIAA, but brain TRP levels were not decreased by the injections. In conclusion, this study demonstrates that brain glucose can act on serotonergic metabolism and thus can prevent exercise‐induced increase of 5‐HT levels. The results also suggest that extracellular brain glucose does not act on the synthesis way of 5‐HT, but probably on the release/reuptake system.     

Association analysis of polymorphisms at the interleukin‐1 locus in essential hypertension

Infection with microorganisms such as Helicobacter pylori and Chlamidia pneumoniae has been associated with coronary heart disease (CAD) and hypertension (HT). Infection increases the release of pro‐inflammatory cytokines, thus facilitating interactions that lead to vascular damage and other effects. We hypothesized that genetically determined differences in activity or responsiveness of cytokine(s) might contribute to HT. The interleukin‐1 gene (IL1) cluster on chromosome 2q14 contains three related genes (IL1A, IL1B, and IL1RN) located within a 430‐kb region. These encode IL‐1α and IL‐1β, as well as their endogenous receptor antagonist, IL‐1ra. The IL1RN gene has a penta‐allelic 86‐bp tandem repeat in intron 2. Allele IL1RN* 2 is associated with a wide range of chronic inflammatory and autoimmune conditions, and its combination with the ? 31T variant of an IL1B C(? 31)T polymorphism constitutes a pro‐inflammatory haplotype that leads to vigorous IL‐1β production. We therefore tested each of these polymorphisms for association with HT. Subjects were white Anglo‐Celtic residents of Sydney, Australia. Frequencies of IL1B C(? 31)T genotypes CC, CT, and TT were 0.50, 0.40, and 0.10 in normotensive (NT) and 0.46, 0.46, and 0.08 in HT, respectively (χ² = 1.2, P = 0.55). T allele frequency in NT (0.30) was similar to that in HT (0.31). For the IL1RN variant, frequencies of alleles IL1RN* 1 and * 2 and combined minor alleles * 3, * 4, and * 5 were 0.61, 0.36, and 0.03 in NT and 0.54, 0.36, and 0.10 in HT, respectively (χ² = 11, P = 0.004). In conclusion, no association of the IL1B C(? 31)T with HT was found, whereas combined frequency of the minor alleles of the IL1RN polymorphism was increased in the HT cohort studied. © 2001 Wiley‐Liss, Inc.     

Respiratory sinus arrhythmia and serotonin transporter promoter gene polymorphisms: Taking a triallelic approach makes a difference

It has been recently reported in Psychophysiology that carriers of the short allele of an insertion/deletion (ins/del) functional polymorphism in the promoter region (5‐HTTLPR) of the serotonin transporter gene may display decreased resting respiratory sinus arrhythmia (RSA). However, this region hosts another functionally connected single‐nucleotide polymorphism (rs25531), which should also be genotyped in order to correctly categorize the low‐ and high‐expressing alleles of 5‐HTTLPR. The present study investigated resting RSA in an ethnically homogenous sample (N = 143) of participants genotyped for both the ins/del and rs25531 polymorphisms in 5‐HTTLPR. In contrast with the biallelic genotypes, based only on the ins/del alleles, the triallelic 5‐HTTLPR genotypes (i.e., including rs25531) showed no association with resting RSA. Taking a triallelic approach to 5‐HTTLPR is thus necessary in order to avoid false positive results.     

Hyperpolarized 13C magnetic resonance spectroscopy detects toxin‐induced neuroinflammation in mice

Lipopolysaccharide (LPS) is a commonly used agent for induction of neuroinflammation in preclinical studies. Upon injection, LPS causes activation of microglia and astrocytes, whose metabolism alters to favor glycolysis. Assessing in vivo neuroinflammation and its modulation following therapy remains challenging, and new noninvasive methods allowing for longitudinal monitoring would be highly valuable. Hyperpolarized (HP) ¹³C magnetic resonance spectroscopy (MRS) is a promising technique for assessing in vivo metabolism. In addition to applications in oncology, the most commonly used probe of [1–¹³C] pyruvate has shown potential in assessing neuroinflammation‐linked metabolism in mouse models of multiple sclerosis and traumatic brain injury. Here, we aimed to investigate LPS‐induced neuroinflammatory changes using HP [1–¹³C] pyruvate and HP ¹³C urea. 2D chemical shift imaging following simultaneous intravenous injection of HP [1–¹³C] pyruvate and HP ¹³C urea was performed at baseline (day 0) and at days 3 and 7 post‐intracranial injection of LPS (n = 6) or saline (n = 5). Immunofluorescence (IF) analyses were performed for Iba1 (resting and activated microglia/macrophages), GFAP (resting and reactive astrocytes) and CD68 (activated microglia/macrophages). A significant increase in HP [1–¹³C] lactate production was observed at days 3 and 7 following injection, in the injected (ipsilateral) side of the LPS‐treated mouse brain, but not in either the contralateral side or saline‐injected animals. HP ¹³C lactate/pyruvate ratio, without and with normalization to urea, was also significantly increased in the ipsilateral LPS‐injected brain at 7 days compared with baseline. IF analyses showed a significant increase in CD68 and GFAP staining at 3 days, followed by increased numbers of Iba1 and GFAP positive cells at 7 days post‐LPS injection. In conclusion, we can detect LPS‐induced changes in the mouse brain using HP ¹³C MRS, in alignment with increased numbers of microglia/macrophages and astrocytes. This study demonstrates that HP ¹³C spectroscopy has substantial potential for providing noninvasive information on neuroinflammation.     

Exercise‐induced changes in brain glucose and serotonin revealed by microdialysis in rat hippocampus: effect of glucose supplementation

The aim of this study was to assess extracellular glucose changes in hippocampus in response to physical exercise and to determine the influence of glucose supplementation. In the same time, we have observed the changes in serotonin, in order to study the relationship between glucose and serotonin during exercise. Both glucose and serotonin were assessed using microdialysis. Exercise induced an increase in extracellular glucose levels over baseline during exercise to 121.1 ± 3.0% (P < 0.001), then a decrease to baseline during recovery. The serotonin followed glucose changes during the first 90 min of exercise, but followed a different pattern during recovery, increasing to a maximum of 129.9 ± 7.0% after 30 min of recovery (P < 0.001). When a 15% glucose solution was infused (10 μL min^–1) during exercise and recovery, blood glucose concentration was increased, but extracellular brain glucose decreased to reach a minimum of 73.3 ± 4.6% after 90 min of recovery (P < 0.001). Serotonin was always the mirror‐reflect of cerebral glucose, with a maximum increase of 142.0 ± 6.9% after 90 min of recovery (P < 0.001). These results show that exercise induces changes in brain glucose and 5‐hydroxytryptamine (5‐HT) levels, which were dramatically modified by glucose infusion. Taking into account the implication of brain 5‐HT in central fatigue, they suggest that if glucose supplementation, before and during exercise, undoubtedly increase performance because of its peripheral positive action, it would have a negative impact on the quality of recovery after the end of the exercise.     

Single-trial electroencephalogram predicts cardiac acceleration: a time-lagged P-correlation approach for studying neurovisceral connectivity

Cortical efferences to the heart are important for cardiovascular health, psychopathology, emotion regulation and other dimensions of human functioning. Although researchers have already begun to outline the underlying neuroanatomy, the timing of neurovisceral communication in humans is difficult to study non-invasively. A possible coupling between the brain and the heart can be observed following feedback stimuli, which have been shown to evoke both, early (i.e. <500 ms) signatures in the electroencephalogram (EEG) and changes in the chronotropy of subsequent heart beats. Because standard approaches may be insufficient to study how these responses are related, we suggest a method termed “Cardio–Electroencephalographic Covariance Tracing” (CECT), which is based on time-lagged P-correlations (i.e., correlations within individuals) between single-trial EEG magnitudes and heart period changes. When CECT was applied to data from n=31 individuals who performed a gambling task, central midline EEG magnitudes from 280 to 340 ms after feedback reliably P-correlated with cardiac acceleration 2 to 5 s thereafter. In addition positive vs. negative feedback lead to enhanced event related potential amplitudes from 200 to 280 ms and to relative cardiac acceleration from 1 to 3.5 s after feedback presentation. The results imply that neurogenic cardiac modulations begin to be affected 200 to 400 ms after stimulus presentation and demonstrate the utility of CECTs for future investigations.     

Obsessive‐Compulsive Disorder in the DSM‐5

Whereas the specific diagnostic criteria for obsessive‐compulsive disorder (OCD) have changed in only minor ways in the transition from DSM‐IV to DSM‐5, a more substantial change is that OCD is no longer classified as an anxiety disorder. Rather, it is now the flagship diagnosis of a new diagnostic category: the obsessive‐compulsive and related disorders (OCRDs). In this article, we describe the nature of obsessional problems as determined through empirical research before turning to a consideration of how OCD is defined in previous editions of the DSM and in DSM‐5. We then critically consider the DSM criteria, as well as the basis for removing OCD from the anxiety disorders and creating the new OCRD category. Finally, we consider the implications of these changes for clinical practice and research on OCD.     

Conditioned and extinguished fear modulate functional corticocardiac coupling in humans

Although the conditioned cardiac fear response is an important index of psychophysiological fear processing, underlying neural mechanisms remain unclear. N = 22 participants underwent differential fear conditioning and extinction with face pictures as conditioned stimuli (CS) and loud noise bursts as aversive unconditioned stimulus (US) on Day 1 and a recall test 1 day later. We assessed ERPs, evoked heart period (HP), and time‐lagged within‐subject correlations of single‐trial EEG amplitude and HP as index for corticocardiac coupling in response to the CS. Fear‐conditioned stimuli (CS+) triggered cardiac deceleration during fear acquisition and recall. Meanwhile, only during Day 1 acquisition, CS+ evoked larger late positivities in the ERP than CS?. Most importantly, during Day 2 recall, stimulus‐evoked single‐trial EEG responses in the time window between 250 and 500 ms predicted the magnitude of cardiac fear responses 2 to 5 s later. This marker of corticocardiac coupling selectively emerged in response to not previously extinguished CS+ but was absent in response to CS? or previously extinguished CS+. The present results provide first evidence that fear conditioning and extinction modulate functional corticocardiac coupling in humans. Underlying mechanisms may involve subcortical structures enhancing corticocardiac transmission to facilitate processing of consolidated conditioned fear.     

Event‐related potentials in response to feedback following risk‐taking in the hot version of the Columbia Card Task

Given the importance of risk‐taking in individuals’ personal and professional life, several behavioral tasks for measuring the construct have been developed. Recently, a new task was introduced, the Columbia Card Task (CCT). This task measures participants’ risk levels and establishes how sensitive participants are to gains, losses, and probabilities when taking risk. So far, the CCT has been examined in behavioral studies and in combination with several (neuro)biological techniques. However, no electroencephalography (EEG) research has been done on the task. The present study fills this gap and helps to validate this relatively new experimental task. To this end, n = 126 students were asked to complete self‐reports (reward responsiveness, impulsiveness, and sensation‐seeking) and to perform the CCT (and other risk tasks) in an EEG setup. The results show that feedback appraisal after risky decision‐making in the CCT was accompanied by a feedback‐related negativity (FRN) and a P300, which were stronger in response to negative than positive feedback. Correlations between the FRN and P300 difference wave on the one hand and risk‐related self‐reports and behavior on the other were nonsignificant and small, but were mostly in the expected direction. This pattern did not change after excluding participants with psychiatric/neurological disorders and outliers. Excluding participants with reversed (positive > negative) difference waves strengthened FRN correlations. The impact such individuals can have on the data should be taken into account in future studies. Regarding the CCT in particular, future studies should also address its oddball structure and its masking of true values (censoring).     

Aggregation Behavior of Poly(3‐hexylthiophene) in Solvent Mixtures: Linear Solvation Energy Relationship (LSER) Modeling and COSMO‐RS Calculations

The solubility and self‐assembly behavior of poly(3‐hexylthiophene) (P3HT) in solvent mixtures, and the dominant intermolecular forces related to these attributes, have only been partially scrutinized. In this work, the extent of aggregation of amorphous P3HT and the structural order of P3HT aggregates (M_n ≈ 20 kDa and M_n ≈ 75 kDa) are investigated in 54 solvent mixtures of chloroform with acetone, acetonitrile, dichloromethane, ethyl acetate, ethanol, and n‐hexane. Correlations between the molecular mass, the extent of aggregation, the structural order of the aggregates, and the nature of the solvent‐P3HT interactions are studied using a (1) linear solvation energy relationship (LSER) modeling and (2) solubility parameter‐based Flory–Huggins interaction parameters, χ. In addition, COSMO‐RS calculations are used to assess correlations between the extent of aggregation and the activity coefficients, γ, of P3HT. The results reveal that the extent of aggregation and the structural order of the P3HT aggregates are governed by different solvent–P3HT interactions. LSER modeling shows that the nucleophilicity and polarity of the solvent blends are the principal determinant of the structural order of P3HT aggregates. This result, which is based on an independent experimental method, supports previous computational results using COSMO‐RS σ‐profiles to assess the nucleophilicity and polarity of the solvent.     

Conversion of Face‐On Orientation to Edge‐On/Flat‐On in Induced‐Crystallization of Poly(3‐hexylthiophene) via Functionalization/Grafting of Reduced Graphene Oxide with Thiophene Adducts

Reduced graphene oxide (rGO) is functionalized with 2‐thiophene acetic acid (rGO‐f‐TAA) and grafted with poly(3‐dodecylthiophene) (rGO‐g‐PDDT) and poly(3‐thiophene ethanol) (rGO‐g‐PTEt) to manipulate the orientation and patterning of crystallized poly(3‐hexylthiophene) (P3HT). P3HT chains prefer to interact with their thiophene rings with bared rGO surface, resulting in a conventional face‐on orientation. In these hybrids, beyond critical length of P3HT nanofibers developed onto rGO (>100 nm), an inclination occurs after solvent evaporation, thereby face‐on noninclined fibers change to edge‐on inclined ones. In P3HT/rGO‐f‐TAA supramolecular structures patterned with P3HT short nanofibrils (42–95 nm in length), the orientation of P3HT chains changes from face‐on to edge‐on, originating from strong interactions between hexyl side chains of P3HTs and 2‐thiophene acetic acid functional groups of rGO. Supramolecular structures based on grafted rGO demonstrate a patched‐like morphology composed of flat‐on P3HTs with main backbones perpendicular to substrate. Grafted polythiophenic oligomers onto rGO (rGO‐g‐PDDT and rGO‐g‐PTEt) provoke P3HT backbones to vertically attach to surface and remain perpendicular even after solvent evaporation. Flat‐on orientation acquired for rGO‐g‐PDDT and rGO‐g‐PTEt systems is the best for P3HT chains assembled onto rGO. Face‐on P3HT/rGO hybrids and, subsequently, edge‐on P3HT/rGO‐f‐TAA hybrids also reflect optical and supramolecular donor–acceptor properties based on ultraviolet–visible and photoluminescence analyses.     

The oft‐neglected role of parietal EEG asymmetry and risk for major depressive disorder

Relatively less right parietal activity may reflect reduced arousal and signify risk for major depressive disorder (MDD). Inconsistent findings with parietal electroencephalographic (EEG) asymmetry, however, suggest issues such as anxiety comorbidity and sex differences have yet to be resolved. Resting parietal EEG asymmetry was assessed in 306 individuals (31% male) with (n=143) and without (n=163) a DSM‐IV diagnosis of lifetime MDD and no comorbid anxiety disorders. Past MDD+ women displayed relatively less right parietal activity than current MDD+ and MDD? women, replicating prior work. Recent caffeine intake, an index of arousal, moderated the relationship between depression and EEG asymmetry for women and men. Findings suggest that sex differences and arousal should be examined in studies of depression and regional brain activity.     

Role of 5‐HT2A, 5‐HT4 and 5‐HT7 receptors in the antigen‐induced airway hyperresponsiveness in guinea‐pigs

Background A possible role of 5‐hydroxytryptamine (5‐HT) in the origin of antigen‐induced airway hyperresponsiveness (AI‐AHR) has been scarcely investigated. Objective To explore the participation of different 5‐HT receptors in the development of AI‐AHR in guinea‐pigs. Methods Lung resistance was measured in anaesthetized guinea‐pigs sensitized to ovalbumin (OVA). Dose–response curves to intravenous (i.v.) acetylcholine (ACh) were performed before and 1 h after antigenic challenge and expressed as the 200% provocative dose (PD₂₀₀). Organ bath experiments, confocal microscopy and RT‐PCR were additionally used. The 5‐HT content in lung homogenates was measured by HPLC. Results Antigenic challenge significantly decreased PD₂₀₀, indicating the development of AI‐AHR. This hyperresponsiveness was abolished by a combination of methiothepin (5‐HT₁/5‐HT₂/5‐HT₅/5‐HT₆/5‐HT₇ receptors antagonist) and tropisetron (5‐HT₃/5‐HT₄ antagonist). Other 5‐HT receptor antagonists showed three different patterns of response. Firstly, WAY100135 (5‐HT_1A antagonist) and ondansetron (5‐HT₃ antagonist) did not modify the AI‐AHR. Secondly, SB269970 (5‐HT₇ antagonist), GR113808 (5‐HT₄ antagonist), tropisetron or methiothepin abolished the AI‐AHR. Thirdly, ketanserin (5‐HT_2A antagonist) produced airway hyporresponsiveness. Animals with bilateral vagotomy did not develop AI‐AHR. Experiments in tracheal rings showed that pre‐incubation with LP44 or cisapride (agonists of 5‐HT₇ and 5‐HT₄ receptors, respectively) induced a significant increase of the cholinergic contractile response to the electrical field stimulation. In sensitized lung parenchyma strips, ketanserin diminished the contractile responses to ACh. Sensitization was associated with a ninefold increase in the 5‐HT content of lung homogenates. Confocal microscopy showed that sensitization enhanced the immunolabelling and co‐localization of nicotinic receptor and 5‐HT in airway epithelium, probably located in pulmonary neuroendocrine cells (PNECs). RT‐PCR demonstrated that neither sensitization nor antigen challenge modified the 5‐HT_2A receptor mRNA levels. Conclusions Our results suggested that 5‐HT was involved in the development of AI‐AHR to ACh in guinea‐pigs. Specifically, 5‐HT_2A, 5‐HT₄ and 5‐HT₇ receptors seem to be particularly involved in this phenomenon. Participation of 5‐HT might probably be favoured by the enhancement of the PNECs 5‐HT content observed after sensitization. Cite this as: P. Segura, M. H. Vargas, G. Córdoba‐Rodríguez, J. Chávez, J. L. Arreola, P. Campos‐Bedolla, V. Ruiz, L. M. García‐Hernández, C. Méndez and L. M. Montaño, Clinical & Experimental Allergy, 2010 (40) 327– 338.     

Use Your Imagination: College Women's Responses to a Social‐Evaluative Body Image Threat

This study examined psychological and heart rate responses to an imagined social‐evaluative body image threat in women (N = 97). Participants were randomly assigned to picture themselves trying on swimsuits in a store with a group of friends (social‐evaluative threat) or alone (non‐social‐evaluative threat). Measures of state body image and heart rate recordings were completed prior to and following the scenario. A significant group‐by‐time interaction was found for state body image, F(2, 93) = 3.69, p = .03, with the highest body shame and social physique anxiety reported in the social‐evaluative group. No differences were found for heart rate. The findings highlight the usefulness of imagined scenarios when examining psychological responses and the challenges of capturing changes in physiological outcomes.     

T cell‐derived leptin contributes to increased frequency of T helper type 17 cells in female patients with Hashimoto's thyroiditis

Leptin modulates T cell function and plays an important role in autoimmune diseases. Our study aimed to explore the role of leptin and T helper type 17 (Th17) cells in Hashimoto's thyroiditis patients. Twenty‐seven patients with Hashimoto's thyroiditis (HT) and 20 healthy controls were enrolled into the current study. A modest increase of plasma leptin in HT patients and the CD4⁺ T cell‐derived leptin from HT patients was stronger than that from healthy controls. In HT patients, there are no statistically significant correlations between plasma leptin concentrations and the percentage of Th17 cells or the level of retinoic acid‐related orphan receptor γt (RORγt), but strong positive correlations were observed between CD4⁺ T cell‐derived leptin and the percentage of Th17 cells or the level of RORγt mRNA, and additionally significantly up‐regulated leptin, interleukin (IL)17 and RORγt mRNA levels in the thyroid tissue. Furthermore, neutralization of leptin decreases the frequency of Th17 cells in vitro. Current study has revealed an increased leptin involvment in Hashimoto's thyroiditis associated with an increased number of Th17 cells.     

Sleep quality and diurnal preference in a sample of young adults: Associations with 5HTTLPR,PER3, and CLOCK 3111

Research investigating associations between specific genes and individual differences with regards to the quality and timing of sleep has primarily focussed on serotonin‐related and clock genes. However, there are only a few studies of this type and most of those to date have not considered the possibility of gene–environment interaction. Here, we describe associations between sleep quality and diurnal preference and three functional polymorphisms: 5HTTLPR, PERIOD3, and CLOCK 3111. Furthermore, we assessed whether associations between genotypes and sleep phenotypes were moderated by negative life events—a test of gene–environment interaction. DNA from buccal swabs was collected from 947 individuals [mean age = 20.3 years (SD = 1.77), age range = 18–27 years; 61.8% female] and genotyped for the three polymorphisms. Participants completed the Pittsburgh Sleep Quality Index and the Morningness‐Eveningness Questionnaire. There was a significant main effect of 5HTTLPR on sleep quality, indicating that “long–long” homozygotes experienced significantly poorer sleep quality (mean = 6.35, SD = 3.36) than carriers of at least one “short” allele (mean = 5.67, SD = 2.96; β = ?0.34, P = 0.005). There were no main effects of 5HTTLPR on diurnal preference; no main effects of PERIOD3 or CLOCK on sleep quality or diurnal preference; and no significant interactions with negative life events. The main effect of the “long” 5HTTLPR allele contradicts previous research, suggesting that perhaps the effects of this gene are heterogeneous in different populations. Failure to replicate previous research in relation to PERIOD3 and CLOCK concurs with previous research suggesting that the effects of these genes are small and may be related to population composition. © 2011 Wiley‐Liss, Inc.     

Temporal stability of regression‐based electrooculographic correction coefficients

A means of accounting for ocular artifact in the electroencephalograph (EEG) is to subtract portions (Bs) of ocular voltage measured by the electrooculograph (EOG) from the EEG. Some such EOG correction methods calculate Bs at one time and use these to correct data recorded at a different time; these require information about the temporal stability of the Bs. This study investigated the stability of Bs over a 2‐hr EEG recording session. Participants performed 5 eye movement tasks, each separated by 30 min. Four EOG correction methods were then used to calculate Bs from each of the 5 data sets, resulting in VEOG, HEOG, and REOG (where appropriate) Bs for each methods at each of the 5 time points. We did not find evidence that Bs changed over the 2‐hr period, nor of any difference in temporal stability between the methods. This study suggests that it is appropriate to employ Bs calculated from calibration trials to correct data recorded within at least a 2‐hr time window.